Evidence map›Paper›PMID 33509641›Full record

ReviewPlacenta2021

Placental blood flow sensing and regulation in fetal growth restriction.

L C Morley, M Debant, J J Walker, D J Beech, N A B Simpson

Open access · hybridAbstract readReview
In one paragraph

Review in Placenta, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Effects of the Supplementation ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. CaBiomedical reports · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

L C MorleyLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, LS2 9DA, UK. Electronic address: l.c.morley@leeds.ac.uk.
M DebantLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, LS2 9DA, UK. Electronic address: m.debant@leeds.ac.uk.
J J WalkerDivision of Women's and Children's Health, School of Medicine, University of Leeds, LS2 9NS, UK. Electronic address: j.j.walker@leeds.ac.uk.
D J BeechLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, LS2 9DA, UK. Electronic address: d.j.beech@leeds.ac.uk.
N A B SimpsonDivision of Women's and Children's Health, School of Medicine, University of Leeds, LS2 9NS, UK. Electronic address: n.a.b.simpson@leeds.ac.uk.
University of Leeds · GB

Funding

British Heart Foundation RG/17/11/33042Medical Research Council MR/P002099/1Wellcome Trust 110044/Z/15/Z
6 · The paper itself

Abstract

The mechanical force of blood flow is a fundamental determinant of vascular homeostasis. This frictional stimulation of cells, fluid shear stress (FSS), is increasingly recognised as being essential to placental development and function. Here, we focus on the role of FSS in regulating fetoplacental circulatory flow, both in normal pregnancy and that affected by fetal growth restriction (FGR). The fetus is reliant on placental perfusion to meet its circulatory and metabolic demands. Failure of normal vascular adaptation and the mechanisms enabling responsive interaction between fetoplacental and maternal circulations can result in FGR. FSS generates vasodilatation at least partly through the release of endothelial nitric oxide, a process thought to be vital for adequate blood flow. Where FGR is caused by placental dysfunction, placental vascular anatomy is altered, alongside endothelial dysfunction and hypoxia, each impacting upon the complex balance of FSS forces. Identifying specific mechanical sensors and the mechanisms governing how FSS force is converted into biochemical signals is a fast-paced area of research. Here, we raise awareness of Piezo1 proteins, recently discovered to be FSS-sensitive in fetoplacental endothelium, and with emerging roles in NO generation, vascular tone and angiogenesis. We discuss the emerging concept that activating mechanosensors such as Piezo1 ultimately results in the orchestrated processes of placental vascular adaptation. Piecing together the mechanisms governing endothelial responses to FSS in placental insufficiency is an important step towards developing new treatments for FGR.

Indexed as

Placental CirculationAnimalsFemaleFetal Growth RetardationFetusHemodynamicsHumansPregnancyUmbilical ArteriesEndothelial cellFlowMechanosensingPiezo1PlacentaShear stress

Identifiers

PMID33509641
PMCPMC8448138
OpenAlexW3125103697

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.